The eating disorders bulimia nervosa and anorexia nervosa are serious psychiatric syndromes affecting 2 to 3 percent of young women, and significant although smaller number of young men. Women with bulimia nervosa or anorexia nervosa manifest abnormalities in regulation of serotonin, a central nervous system (CNS) neurotransmitter involved in regulation of food intake, mood and impulsive/obsessional behaviors. The goal of the current project is to evaluate whether abnormalities in serotonin regulation reflection reflect trait-related characteristics present in individuals who develop an eating disorder. Recurrent dieting is a frequent precursor to bulimia nervosa and anorexia nervosa. In healthy controls, dieting decreases blood tryptophan levels, resulting in an apparent decrease in CNS serotonin synthesis. Normally, serotonergic pathways are though to respond to dieting through augmentation of post-synaptic receptor responsiveness. It is hypothesized that in women with a neurobiological predisposition to eating disorders, CNS receptors are not able to respond adequately to compensate for diet-associated decreases in serotonin synthesis. This deficiency could contribute to the onset of eating disorder symptoms. Study groups will include women who have recovered from bulimia nervosa, women who have recovered from anorexia nervosa, and healthy female controls. Based on a randomized, controlled, crossover design, subjects will participate in low-tryptophan and normal tryptophan eight-day study diets. In comparison to results in controls, the long-term remitted patient groups are anticipated to respond to a low-tryptophan diet with significantly impaired diet-induced augmentation of dexfenfluramine-stimulated prolactin response. Indirect measures of physiological/metabolic response to dietary changes, including blood leptin concentration, will be compared across study groups. These studies will provide important new information on the potential roles of dieting and serotonin in the development of eating disorders.